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132 Cards in this Set

  • Front
  • Back
monckeberg arteriosclerosis
- medial calcific sclerosis
- involves radial and ulnar arteris
- >50 yrs old
> does not obstruct arterial flow b/c intima is not involved
- ring-like calcifications of the media
- get 'pipestem' arteries
define arteriosclerosis
- general term for three types of vascular disease
- characterized by rigidity (sclerosis) and thickening of blood vessels
1. monckeberg arteriosclerosis
2. arteriolosclerosis
3. artherosclerosis
- hyaline thickening or changes of the small arteries and arterioles (usually in kidnies)
- associated wtih hypertension or DM
1. Hyaline arteriolosclerosis
2. hyperplastic arteriolosclerosis
hyaline arteriolosclerosis
- hyaline thickening of arteriolar walls
- called 'benign nephrosclerosis' in the kidnies and is associated with hypertension
hyperplastic arteriolosclerosis
- concnetric, laminated 'onion skin' thickeining of arteriolar walls
- may be seen with necrotizing arteriolitis
- called 'malignant nephrosclerosis' in the kidneys -> associated with malignant hypertension
what is necrotizing arteriolitis
intramulra deposition of fibrinoid material in arterioles with vascular necrosis and inflammation
what are the three layers of the vascular wall?
1. intima
2. media
3. adventitia
where is the principal point of resistance to blood flow found?
- arterioles
- resistance is inversely proportional to the fourth power of the diameter
describe the structure of capillaries
- endothelial lining, but no media
how much of total body blood is found in the veins?
where is von Willebrand factor found?
- in the Weibel-Palade bodies in endothelial cells
what happens if you have frank loss (denudation) of EC?
- thrombosis and SCM proliferation
describe the characteristics of atheroscelosis
- atheromas occur in the intima of arteries
1. the atheromas have a central core of cholesterol and CEs, foam cells, Ca, and necrotic debris
2. core is covered by a fibrous cap
3. can develop from fatty streaks
what is an atheroma?
fibrous plaque
what are fibrous caps made out of?
- smooth muscle cells
- foat cells
- fibrin
- coagulation proteins
- extracellular matrix: collagen, elastin, glycosaminoglycans, and proteoglycans
describe a fatty streak
- focal accumulations in the intima of lipid-laden foam cells that may appear at very young ages (1st year of life) and is seen in the aorta of most older children
how might artheromas be complicated?
- ulceration, hemorrhage into the plaque, or calcification of the plaque
- thrombus formation
- embolization of an overlying thrombus, or plaque material itself
what are the consequences of artherosclerosis?
- ischemic heart disease and MI
- stroke, ischemic bowel disease, peripheral vascualr occlusive disease
- renal arterial ischemia with secondary hypertension
- aneurysm from weakened arterial walls
what are the risk factors for atherosclerosis?
- age
- male gender
- increased in postmenopausal women
- hypercholesterolemia
where do you get serum cholesterol from?
- dietary, exogenous
- biosynthetic, endogenous
what is the clinical predictor of atherogenesis?
- relative concentrations of lipoprotein fractions
- ideally, LDL to HDL should be 4:1
additional risk factors for atherosclerosis
- hypertension
- DM
- Cigarettes
- obesity, physical inactivity, type a personality, hyperuricemia, hyperhomocysteinemia, methylene tetrahydrofolate reductase mutations, lipoprotein A, C. pneumoniae, OCPs
atherosclerotic peripheral vascular occlusive disease
- often seen in DM.
- leads to gangrene of the LE
what is the insudation hypothesis of atherosclerosis?
- infiltration of teh intima with lipid and protein is teh primary artherogenic event
what is the encrustation or thrombogenic hypothesis?
- prganization of repeated mural thrombi on the intimal surface leads to buildup of plaques filled with lipid derived from the breakdown of platelets and leukocytes
what is the monoclonal hypothesis?
- smooth muscle migration and proliferation is analogous to tumor growth, and is the primary rather than secondary event.
- smooth muscle prolifertaion in atheromas are often monoclonal
- hyperlipidemia may incite proliferation
current views on artherosclerosis
(primary event)
- primary event is injury to the endothelium (from hypercholesterolemia, mechanical injury, hypertension, immune mech, toxins, or infectious agents
- hyperlipidemia may initiate endothelial injury, promote foam cell formation
what happens after the primary event in artherosclerosis?
1. entry of monocytes and lipid into the subendothelium, sometimes with platelet adhesion and aggregation at the injury site
2. mitogenic factors are released from platelets
3. groth and proliferatin of smooth muscle cells into the intima
4. monocyte conversion into foam cells is mediated by the b-VLDL receptor and the scavenger receptor, which recognizes modified LDL
name some mitogenic factors
- TGF-a
- released from platelets and possibly monocytes
list the different types of aneurysms
1. atherosclerotic aneurysms
2. aneurysms due to cystic medial necrosis
3. berry aneurysms
4. syphilitic (luetic) aneurysm
5. dissctive aneurysm (dissecting hematoma)
6. arteriovenous fistula (aneurysm)
atherosclerotic aneurysms
- found in descendin, esp abdominal aorta
aneurysms due to cystic medial necrosis
- most frequent aneurysms of the aortic root
berry aneurysms
- saccular, small lesions seen in the smaller arteries of the brain (esp. the circle of Willis)
- not related to atherosclerosis
- not present at brith, but develop at sites of congenital medial weakness (e.g. bifurcations of cerebral arteries)
what are berry aneurysms often associated with?
- polycystic kidney disease
syphilitic (luetic) aneurysm
- teritary syphillis
- caused by syphilitic aortitis- obliterative endarteritis of the vasa vasorum and necrosis of the media
- you get 'tree-bark' appearance
- usually invovle the ASCENDING aorta --> may widen the aortic commisures --> AV insufficiency
dissecting aneurysm
- dissecting hematoma
- longitudinal intraluminal tear usually in the wall of the ascending aorta
- associated with hypertension or with cystic medial necrosis
- end result: arotic rupture into the pericardial sac, causing hemopericardium and fatal caridac tamponade
what are some of the clinical symptoms of dissecting aneurysms?
- severe, tearing chest pain, often radiating through to the back
- radiograph may show widening of aortic shadow
how do you differentiate a dissecting aneurysm from MI?
- ECG, serum troponin I, and serum myocardial enzymes are normal
arteriovenous fistula
- abnormal communication between an artery and vein
- can be secondary to trauma
- causes ischemic changes from the diversion of blood, ballooning and aneurysm formation from increased venous pressure, high output cardiac failure from hypervolemia
venous thrombosis (phlebothrombosis)
- arises from the deep veins of the lower extremities
- associated wtih inflammation -> thrombophlebitis
- risk factors: venous circulatory stasis, partially obstructed venous return (as seen in cardiac failure, preganncy, prolonged bed rest, or varicose veins)
describe PEs
- hemorrhagic
- subpleural
- wedge shaped
what are risk factors for varicose veins?
- increased venous pressure as seen in:
- pregnancy, obesity, thrombophlebitis, and occupations where you are often standing
what is a hamartoma?
A hamartoma is a common benign tumor in an organ composed of tissue elements normally found at that site but that are growing in a disorganized mass. Hamartomas result from an abnormal formation of normal tissue, although the underlying reasons for the abnormality are not fully understood. They grow along with, and at the same rate as, the organ from whose tissue they are made, and, unlike cancerous tumors, only rarely invade or compress surrounding structures significantly.
benign vascular tumors
- not true neoplasms. gnerally better characterized as malformations or hamartomas
1. spider telangiectasia
2. hereditary hemorrhagic telangiectasia
3. hemangioma (angioma)
4. Glomangioma
5. cystic hygroma
spider telangiectasia
- dilated small vessel surrounded by radiating final channels
- associated with hyerestrinism (seen in chronic liver disease and pregnancy)
what is hyperestrinism?
- hyperestrogenism
hereditary hemorrhagic telangeictasia
- osler-weber-rendu syndrome
- autosomal dominant condition
- local dilation and convolution of venules and capillaries of the skin and mucous membranes
- complicated by epistasis or GI bleeding
define epistaxis
- angioma
- malformation of a larger vessel composed of masses of channels filled with blood
- most common tumor of infancy
- port-wine stain birthmarks
1. capillary hemangioma
2. cavernous hemangioma
capillary hemangioma
- closely packed capillary-like channels in the skin, subcutaneous tissues, lips, liver, spleen or kidneys
cavernous hemangioma
- large cavernous vascualr spaces in the skin and mucosal surfaces in the liver, pancreas, spleen, and brain
- can be seen in von Hippel Lindau disease
what is von Hippel Lindau disease?
- autosomal domainant
- marked by hemangioblastomas of the cerebellum, brain stem, retina
- adenomas and cysts of the liver, kidney, pancreas
define: adenoma
This term is applied to a tumour, usually benign, in glandular tissue.
- glomus tumor
- small, purplish, painful subungual nodule of the finger or toe
define: subungual
Beneath a fingernail or toenail.
cystic hygroma
- lymphangioma that occurs in the neck or axilla
list the malignant vascular tumors
1. hemangioendothelioma
2. hemangiopericytoma
3. hemangiosarcoma (angiosarcoma)
4. Kaposi sarcoma
- intermediate in behavior between a benign and malignant tumor
- comes from pericytes
- varies in behavior between benign and malignant
- antiosarcoma
- rare, malignant, vascular tumor found in the skin, musculo-skeletal system, breast and liver
- associated with toxic exposure to arsenic, or thorium dioxide (thorotrast- a contrast agent)
- polyvinal chloride (PVC) is asociated with hemangiosarcomas of the liver
kaposi sarcoma
- malignant vascular tumor
- classic form: found in older ashkenazi or mediterranean men
- endemic (African) KS- affects younger african men and children
- epidemic KS: seen in AIDS patients. caused by KS herpesvirus
what accounts for as many as 10% of all cancers in Africa?
kaposi sarcoma
vasculitis syndromes
- inflammatory and often necrotizing
- mediated my immune mechanisms (e.g immune complex depositions)
- frequent antigens in complexes: DNA, hep B surface antigen, and hep C RNA
List the vasculitides
1. Polyarteritis nodosa
2. Churg- Strauss syndrome
3. Hypersensitivity vasculitis
4. Wegener granulomatosis
5. Giant cell artertides
6. Mucocutaneous lymph node syndrome
7. Thromboangiitis obliterans
8. Lymphomatoid granulomatosis
Polyarteritis nodosa
- necrotizing immune complex inflammation of small and medium sized arteries
- aneurysmal nodules form from descrtruction of arterial medial and internal elastic lamella
what is polyarteritis nodosa associated with?
- hep B
- seen in 30% of patients
what are the clinical manifestations of polyarteritis nodosa?
- fever, weight loss, malaise, abdominal pain, headache, myalgia, hypertension
where is polyarteritis nodosa found?
1. kidneys: immune complex vasculitis in the arterioles and glomeruli, renal lesions and hypertension -> death
2. coronary arteries -> ischemic HD
3. MS system -> myalgia, arthralgia, arthritis
4. GI -> nausea, vomiting, ABDOMINAL PAIN
5. CNS or PNS, eye, or skin
define arthralgia
joint pain
what do lab studies show in polyarteritis nodosa?
- serum antibodies to neutrophilic myleoperoxidases (P-ANCAs: perinuclear antineutrophil cytoplasmic antibodies)
Churg- Strauss syndrome
- allergic granulomatous angiitis
- necrotizing vasculitis that is a variant of polyarteritis nodosa
- involves pulmonary vasculature, marked peripheral eosinophilia, and clinical manifestation of asthma
Hypersensitivity vasculitis
- aka leukocytoclastic vasculitis
- immune complex-mediated vascultides characterized by acute inflammation of small blood vesels
- mutiple lesions are of the same age (not the case in polyarteritis nodosa!)
what is the clinical manifestation of hypersensitivity vasculitis?
- palpable purpura when skin is involved
- Honoch- Schonlein purpura
- Serum sickness
what can precipitate hypersensitivity vasculitis?
- exogenous antigens: drugs, foods, infectious stuff
- may also come on as a complication of systemic illness (e.g. connective tissue disorders or malignancies)
describe Honoch-Schonlein purpura in hypersensitivity vasculitis
- hemorrhagic urticaria of extensor surfaces of the arms, legs, and buttocks, with fever, arthralgias, and GI and renal involvement (similar to IgA nephropathy)
- can be poststreptococcal in origin
- associated with antecedent URIs
describe serum sickness in hypersensitivity vasculitis
- caused by therapeutic administration of various antitoxins (e.g. from horses)
wegener granulomatosis
- unknown etiology
- characterized by necrotizing granulomatous vasculitis of small to medium sized vessesl of the respiratory tract, kidneys and other organs
describe wegenier granulomatosis clinically
- dominated by respiratory tract signs and symptoms, especially of the paranasal sinuses and lungs, and necrotizing glomerulonephritis
- fibrinoid necrosis of small arteries and veins
- early infiltration by neutrophils
- granuloma formation with giant cells
what do you find with wegener granulomatosis?
- circulating antineutrophil cytoplasmic antiboides witha cytoplasmic staining pattern (C-ANCAs)
where do you find C-ANCAs? and P-ANCAs?
C-ANCAs: wegener granulomatosis
P-ANCAs: polyarteritis nodosa
giant cell arteritides
- seen in medium to large sized arteries
- granuloma formation with giant cells and by infiltrats of mononuclear cells, PMNs, and eosinophils
1. Temporal arteritis
2. Takayasu arteritis
how do endothelial cells affect the reactivity of the underlying smooth muscle cells?
release of
1. relaxing factor (nitric oxide)
2. contracting factor (endothelin)
define endothelial dysfunction
- altered phenotype that impairs vasoreactivity or induces a surface that is thrombogenic
describe the SMC response to injury
- migrate to the intima and proliferate
name the promoters of SMC proliferation and migration
- endothelin-1
- thrombin
- IFN-g
- IL-2
name the inhibitors of SMC proliferation and migration
- heparin sulfates
- NO
- TGF-b
what are the main consequences of atherosclerosis?
- MI, cerebral infarct, aortic aneurysms, peripheral vascular disease
describe the outcomes of the three possibilities in the clinical phase of artherosclerosis
1. aneurysm and rupture
2. occlusion by thrombus
3. critical stenosis
what are the most heavily involved vessels in artherosclerosis in descending order?
1. abdominal aorta
2. coronary arteries
3. popliteal arteries
4. internal carotid arteries
5. vessels of the circle of willis
what type of molecule is needed for binding of leukocytes to andothelial cells?
- after monocytes adhere to the endothelium, they
1. migrate between ECs to localize in the intima
2. transform into macrophages and engulf lipoproteins (oxidized LDL)
describe dyslipoproteinemias
- increased LDL
- decreased HDL
- increased levels of abnormal lipoprotein (Lp)
what causes dyslipoproteinemias?
- mutation yielding defective apolipoprotiens
- nephrotic syndrome
- alcoholism
- hypothyroidism
- DM
familial hypercholesterolemia
- defects in the LDL receptor -> inadequate hepatic LDL uptake -> increased circulating [LDL]
which organisms are suspect in causing atherosclerosis?
- chlamydia pneumonia
- both organisms are widley distributed, can inect cells of the blood vessel wall, and exhibit persistene, latency, and recurrence of infection
define hypertension
systolic > 130
diastolic > 80
what percentage of hypertension is primary hypertension?
- idiopathyic
- no short- term problems
- usually benign unless a MI, cerebrovascular accident, or other compliation comes up
what percentage of hypertension is secondary hypertension?
- 5%
- if untreated, leads to death within 1-2 years
- aka malignant or accelerated hypertension
- clinically: 200/120
renovascular hypotension
- renal artery stenosis -> decreased GFR and pressure -> renin secretion -> angiotensin II mediated vasoconstriction and increased peripheral resistance -> increased Na reabsorption -> more blood volume
eqn for blood pressure
how is TPR regulated?
- primarily at the level of the arterioles
- influenced by neural and hormonal factors
name some humoral vasoconstricting factors
- angiotensin II
- catecholamines
- endothelin
name some humoral vasodilating factors
- kinins
- prostaglandins
- NO
describe the effects of low blood volume on sodium
- GFR falls -> sodium reabsorption by the renal proximal tubules is increased
list three factors that influence Renin secretion
- renal artery stenosis
- renin-secreting tumor
- firbomuscular dysplasia
list two factors that influence angiotensinogen production
- OCPs
- angiotensiogen variants
list four factors that influence mineralocorticoid secretion
- aldosteronoma
- GRA (aldosterone synthase)
- 11b- hydroxylase deficinecy
- 17a- hydroxylase deficiency
list four factors that influence mineralocorticoid receptor activity
- licorice
- cushing syndrome?
- AME (11-b HSD)
- Glucocorticoid resistance
what site in the kidney determines net sodium balance?
- the ENaC (epithelial Na- channel) in the corticla collecting duct is regulated by the renin-angiotensin system.
- it regulates the absorption of the last 2% of sodium
temporal arteritis
- most frequent form of vasculitis
- systemic
- found in the elderly
- affects branches of the carotid
what are the clinical manifestations of termporal arteritis?
- malaise, fatigue
- headache, or claudition of the jaw
- tenderness, absent pulse, palpable nodules along the course of the artery
- visual impairment
- polymyalgia rheumatica
- elevated sedimentation rate
what is polymalgia rheumatica?
- complex set of symptoms including proximal muscle pain, periarticular pain, and morning stiffness
takayasu arteritis
- aka pulseless disease
- inflammation and stenosis of medium and large sized arteries, wtih involvement of aortic arch and its branches -> aortic arch syndrome
what are the clinical manifestations of takayasu arteritis?
- basent pulses in carotid, radial, or ulnar arteries
- nonspecific findings such as fever, night sweats, maliase, myalgia, arthritis and arthralgia, eye problems and painful skin nodules
mucocutaneous lymph node syndrome
aka: Kawasaki disease
- acute, self-limited illness of infants and young children
- acute necrotizing vasculitis of small and medium sized vessels
what are the clinical manifestations of mucocutaneous lymph node syndrome?
- fever, hemorrhagic edema of conjunctiva, lips and orla mucosa; cervical lymphadenopathy
- can be a cause of coronry artery vasculitis with aneurysm formation
throboangiitis obliterans
- aka Buerger disease
- acute inflammation involving small- to medium sized arteries of the extremities, extending to adjacent veins and nerves
- jewish more common
- young men more common
what are the end points of thorboangiitis obliterans?
- painful ischemic disease -> gangrene
- exacerbated by heavy cigarette smoking
lymphomatoid granulomatosis
- rare granulomatous vasculitis
- infiltration by atypical lymphocytoid and plasmacytoid cells
- may progress from a chronic inflammatory condition to a fully developed lymphoproliferative neoplasm, esp a T-cell non-hodgkin lymphoma
raynaud disease
- recurrent vasospasm of small arteries and arterioles -> pallor or cyanosis
- esp in fingers and toes
- young healthy women
- preciptated by chilling
raynaud phenomenon
- clinically similar to raynaud's disease, but secondary to an underlying disorder, like:
- progressive systemic sclerosis (scleroderma)
determinants of essential hypertension
- genetic
1. family history (seen in 75% of patients)
2. more comon and more severe in blacks
- environmental factors
1. dietary sodium intake
2. stress (neurogenic vasoconstriction)
3. obesity, cigarette smoking, and physical inactivity
what is the end point of essential hypertension?
- lead to retinal changes, LV hypertrophy, cardia failure, and bening nephrosclerosis
- can predispose to ischemic heart disease or stroke
what is the most common cause of secondary hypertension?
renal disease
causes of renal hypertension
1. disorders of renal parenchyma
2. unilateral renal artery stenosis -> atrophy of kidney and can be surgically corrected
what is the mechanism of renal hypertension?
- juxtaglomerular cells detect lower vascular tone -> secrete renin -> angiotensiogen -> angiotensin I, which is converted to angiotensin II by ACE -> aldosterone (Na retention) and increase in TPR
what are the two ways in which angiotensin II promote hypertension?
- vasoconstrictor
- activator of aldosterone secretion
causes of endocrine hypertension
- primary aldosteronism, or Conn syndrome
- acromegaly, cushing syndrome of pit or adrenocortical origin, phochromocytoma, and hyperthyrodism
- DM
what serum effects do you see with primary aldosteronism?
- aka Conn syndrome
- increased serum Na
- reduced serum K
what are other causes of secondary hypertension?
- coarctation of the aorta -> causes hypertension limited to the upper body
- toxemia of pregnancy
- CNS disorders (brain tumors)
- drugs and chemicals (amphetamines and steroids)
what is malignant hypertension?
- can be derived either from primary or secondary hypertension
- has an accelerated clinical course
- occurs in less than 5% of patients with elevated BP (mostly in young AA males)
what are the clinical symptoms of malignant hypertension?
- increase in diastolic blood pressure
- focal retinal hemorrhages
- papilledema
- LV hypertrophy, LV failure
- results in early death from CHF, cerebrovascular accident, or renal failure
what causes malignant nephrosclerosis?
- malignant hypertension
- arterioles or glomerular capillaries rupture -> 'flea-bitten kidney', multiple pinpoint petechial hemorrhages on surface, large swollen kidneys, necrotizing arteriolitis and glomerulitis with fibrinoid necrosis, hyperplastic arteriolosclerosis, affecting both comeruli and arterioles